The investigator is currently a third year General Surgery resident at the University of California-San Francisco. By elucidating the molecular aspects of wound healing it may be possible to alter the pathways of chronic wounds to heal with better efficiency and provide better therapy for patients with non-healing wounds. Heat shock proteins (Hsp's) are expressed in ischemic wounds. We hypothesize that increased expression of Hsp 32 in wounds is critical to healing of ischemic wounds. Our hypothesis will be studied both in vivo an in vitro. Hsp 32 expression will be determined in ischemic and non-ischemic wounds in animals and in cells cultured in normoxia and hypoxia. Hsp 32 levels will be increased or decreased and the effect on healing of an ischemic wound determined in animals. Levels of hsp 32 will also be altered in cells grown in hypoxia to determine its role in the function of cells. In addition, we plan to study the healing of the ischemic wound in mice that cannot express hsp 32 (HO-1 -/-). Cells from these mice will also be placed in hypoxic conditions and cellular function determined.